Abstract

Several published biologic times for the stage conversion of Toxoplasma gondii from tachyzoite to bradyzoite in mice are critically examined. There are several reports of 3 days and many of longer times. Possible errors, related to delay from dissemination of the infection, are pointed out. The time to the appearance of the 36-kDa surface antigen, sometimes used for the diagnosis of bradyzoites, should be compared with the biologic attribute of bradyzoites, inducing the short prepatent period in cats. It is recalled that the development of acid pepsin resistance is not exclusively correlated with the biologic definition of bradyzoites. Reactivation of toxoplasmosis in mice does not necessarily follow the administration of a corticosteroid. The daily dose, the type of corticosteroid, its solubility, whether alcohol or ester, the route of administration, the host, and, probably, other factors are important in giving rise to sufficient immunosuppression for reactivation to occur. The plea is made to examine biologic measurements in the context of parasitologic and host factors.

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